关键词: 阻塞性睡眠呼吸暂停低通气综合征, 大蒜素, 晚期糖基化终末产物, 糖基化终末产物受体, 核转录因子

Abstract: Objective To investigate the effect of allicin on the reduction of learning ability and hippocampal neuronal apoptosis of obstructive sleep apnea-hypopnea syndrome (OSAHS) in rats. Methods The rats were divided into control group, model group, low-dose(10 mg/kg) and high-dose(40 mg/kg) of allicin group as well as positive drug group (modafinil, 20 mg/kg) with 18 in each. Morris water maze method was used to evaluate the learning ability of rats. HE and TUNEL staining microscopy was used to observe hippocampal tissue lesions and neuron apoptosis index (AI). ELISA method was used to detect tumor necrosis factor(TNF-α) and interleukin-6(IL-6) and advanced glycation end products (AGEs)in hippocampal tissue. RT-qPCR was used to detect advanced glycosylation end product-specific receptor (RAGE), nuclear transcription factor κB(NF-κB) p65, B cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein(Bax) mRNA expression. Western blot was used to detect RAGE, NF-κB p65, p-NF-κB p65, Bcl-2 and Bax protein. Results Compared with the control group, the escape latency was longer, travel time was shorter, cross-platform times was reduced. The expressions of TNF-α, IL-6, AGEs, AI, RAGE, Bax mRNA and RAGE, p-NF-κB p65, Bax protein were increased while Bcl-2 mRNA and protein expression decreased in the model group(P＜0.05). Compared with the model group, the above changes in the low-dose, high-dose allcin and positive drug group were significantly alleviated. HE results showed that the damage of hippocampal neurons in each treatment group was significantly mitigated. Conclusions Allicin can effectively improve learning ability and reduce apoptosis of hippocampal neurons in OSAHS rats, which may play a role through AGEs-RAGE/NF-κB axis and apoptosis-related mRNA and protein expression.

Key words: obstructive sleep apnea hypopnea syndrome, allicin, advanced glycation end products, glycosylation end product receptor, nuclear transcription factor